Monoamine Metabolism in Rat Brain after Increased Intracranial Pressure
Recent animal experiments demonstrate that considerable restitution of cerebral function and metabolism can occur even after prolonged interruption of cerebral circulation. In barbiturate-anaesthetized cats HOSSMANN and SATO (1970) (1) recorded reappearance of the EEG and of evoked cortical potentials after 30–60 minutes of complete cerebral ischemia. In rats under nitrous oxide anaesthesia circulatory interruption for 15 minutes is followed by rapid rephosphorylation of adenine nucleotides and disappearance of accumulated lactate (2). Metabolic signs of restitution of energy metabolism appear long before the EEG returns towards normal patterns (3). Furthermore, neurological function may be grossly abnormal even when considerable restitution of EEG and energy metabolism is at hand (4). These results indicate that tissue alterations other than energy failure may underlie the functional deficits.
KeywordsIschemia Histamine Noradrenaline Neurol Tryptophan
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